mTOR signaling mediates effects of common gamma-chain cytokines on T cell proliferation and exhaustion: implications for HIV-1 persistence and cure research.
Identifieur interne : 000422 ( Main/Exploration ); précédent : 000421; suivant : 000423mTOR signaling mediates effects of common gamma-chain cytokines on T cell proliferation and exhaustion: implications for HIV-1 persistence and cure research.
Auteurs : Harry E. Taylor [États-Unis] ; Nina A. Calantone ; Richard T. D'AquilaSource :
- AIDS (London, England) [ 1473-5571 ] ; 2018.
Descripteurs français
- KwdFr :
- Adulte (MeSH), Cytokines (métabolisme), Humains (MeSH), Infections à VIH (anatomopathologie), Infections à VIH (virologie), Lymphocytes T (immunologie), Lymphocytes T (physiologie), Prolifération cellulaire (MeSH), Sous-unité gamma commune aux récepteurs des interleukines (métabolisme), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (MeSH), VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (croissance et développement), VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (immunologie).
- MESH :
- anatomopathologie : Infections à VIH.
- croissance et développement : VIH-1 (Virus de l'Immunodéficience Humaine de type 1).
- immunologie : Lymphocytes T, VIH-1 (Virus de l'Immunodéficience Humaine de type 1).
- métabolisme : Cytokines, Sous-unité gamma commune aux récepteurs des interleukines, Sérine-thréonine kinases TOR.
- physiologie : Lymphocytes T.
- virologie : Infections à VIH.
- Adulte, Humains, Prolifération cellulaire, Transduction du signal.
English descriptors
- KwdEn :
- Adult (MeSH), Cell Proliferation (MeSH), Cytokines (metabolism), HIV Infections (pathology), HIV Infections (virology), HIV-1 (growth & development), HIV-1 (immunology), Humans (MeSH), Interleukin Receptor Common gamma Subunit (metabolism), Signal Transduction (MeSH), T-Lymphocytes (immunology), T-Lymphocytes (physiology), TOR Serine-Threonine Kinases (metabolism).
- MESH :
- chemical , metabolism : Cytokines, Interleukin Receptor Common gamma Subunit, TOR Serine-Threonine Kinases.
- growth & development : HIV-1.
- immunology : HIV-1, T-Lymphocytes.
- pathology : HIV Infections.
- physiology : T-Lymphocytes.
- virology : HIV Infections.
- Adult, Cell Proliferation, Humans, Signal Transduction.
Abstract
: Chronic elevation of plasma cytokines is a key feature of HIV infection. The physiological consequences of this response to infection and its role in HIV persistence are not fully understood. Here, we show that common gamma chain (γc)-cytokines induce both proliferation and expression of T cell exhaustion markers in a mammalian target of rapamycin (mTOR)-dependent fashion, suggesting a possible therapeutic target that, if inhibited, could diminish HIV reservoir expansion, persistence, and resistance to immune surveillance.
DOI: 10.1097/QAD.0000000000001997
PubMed: 30234610
PubMed Central: PMC6475455
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Taylor</name><affiliation wicri:level="3"><nlm:affiliation>Division of Infectious Diseases and HIV Translational Research Center, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Infectious Diseases and HIV Translational Research Center, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago</wicri:regionArea><placeName><settlement type="city">Chicago</settlement><region type="state">Illinois</region></placeName></affiliation></author><author><name sortKey="Calantone, Nina A" sort="Calantone, Nina A" uniqKey="Calantone N" first="Nina A" last="Calantone">Nina A. Calantone</name></author><author><name sortKey="D Aquila, Richard T" sort="D Aquila, Richard T" uniqKey="D Aquila R" first="Richard T" last="D'Aquila">Richard T. 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D'Aquila</name></author></analytic><series><title level="j">AIDS (London, England)</title><idno type="eISSN">1473-5571</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult (MeSH)</term><term>Cell Proliferation (MeSH)</term><term>Cytokines (metabolism)</term><term>HIV Infections (pathology)</term><term>HIV Infections (virology)</term><term>HIV-1 (growth & development)</term><term>HIV-1 (immunology)</term><term>Humans (MeSH)</term><term>Interleukin Receptor Common gamma Subunit (metabolism)</term><term>Signal Transduction (MeSH)</term><term>T-Lymphocytes (immunology)</term><term>T-Lymphocytes (physiology)</term><term>TOR Serine-Threonine Kinases (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte (MeSH)</term><term>Cytokines (métabolisme)</term><term>Humains (MeSH)</term><term>Infections à VIH (anatomopathologie)</term><term>Infections à VIH (virologie)</term><term>Lymphocytes T (immunologie)</term><term>Lymphocytes T (physiologie)</term><term>Prolifération cellulaire (MeSH)</term><term>Sous-unité gamma commune aux récepteurs des interleukines (métabolisme)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Transduction du signal (MeSH)</term><term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (croissance et développement)</term><term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Interleukin Receptor Common gamma Subunit</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Infections à VIH</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1)</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>HIV-1</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Lymphocytes T</term><term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1)</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>HIV-1</term><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term><term>Sous-unité gamma commune aux récepteurs des interleukines</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>HIV Infections</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Lymphocytes T</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à VIH</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>HIV Infections</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Cell Proliferation</term><term>Humans</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Humains</term><term>Prolifération cellulaire</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">: Chronic elevation of plasma cytokines is a key feature of HIV infection. The physiological consequences of this response to infection and its role in HIV persistence are not fully understood. Here, we show that common gamma chain (γc)-cytokines induce both proliferation and expression of T cell exhaustion markers in a mammalian target of rapamycin (mTOR)-dependent fashion, suggesting a possible therapeutic target that, if inhibited, could diminish HIV reservoir expansion, persistence, and resistance to immune surveillance.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30234610</PMID><DateCompleted><Year>2019</Year><Month>11</Month><Day>04</Day></DateCompleted><DateRevised><Year>2020</Year><Month>11</Month><Day>12</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1473-5571</ISSN><JournalIssue CitedMedium="Internet"><Volume>32</Volume><Issue>18</Issue><PubDate><Year>2018</Year><Month>11</Month><Day>28</Day></PubDate></JournalIssue><Title>AIDS (London, England)</Title><ISOAbbreviation>AIDS</ISOAbbreviation></Journal><ArticleTitle>mTOR signaling mediates effects of common gamma-chain cytokines on T cell proliferation and exhaustion: implications for HIV-1 persistence and cure research.</ArticleTitle><Pagination><MedlinePgn>2847-2851</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1097/QAD.0000000000001997</ELocationID><Abstract><AbstractText>: Chronic elevation of plasma cytokines is a key feature of HIV infection. The physiological consequences of this response to infection and its role in HIV persistence are not fully understood. 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Calantone</name><name sortKey="D Aquila, Richard T" sort="D Aquila, Richard T" uniqKey="D Aquila R" first="Richard T" last="D'Aquila">Richard T. D'Aquila</name></noCountry><country name="États-Unis"><region name="Illinois"><name sortKey="Taylor, Harry E" sort="Taylor, Harry E" uniqKey="Taylor H" first="Harry E" last="Taylor">Harry E. Taylor</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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